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논문 기본 정보

자료유형
학술저널
저자정보
Jin Nam Kim (The Catholic University of Korea) Sung Nim Han (Seoul National University) Tae Joung Ha (Rural Development Administration (RDA)) Hye-Kyeong Kim (The Catholic University of Korea)
저널정보
대한지역사회영양학회 Nutrition Research and Practice Nutrition Research and Practice Vol.11 No.5
발행연도
2017.10
수록면
357 - 364 (8page)

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BACKGROUND/OBJECTIVES: Oxidative stress is closely related with inflammation and development of many diseases. Black soybean seed coat contains high amount of anthocyanins, which are well-known for free radical scavenging activities. This study investigated inflammatory response and action mechanism of black soybean anthocyanins with regard to antioxidant activity in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells.
MATERIALS/METHODS: RAW 264.7 cells were treated with anthocyanins extracted from black soybean seed coats in a concentration range of 12.5 to 100 μg/mL. The production of reactive oxygen species (ROS), secretion of pro-inflammatory mediators and cytokines, and the signaling in the mitogen activated protein kinases (MAPKs) pathway were examined.
RESULTS: Black soybean anthocyanins significantly decreased LPS-stimulated production of ROS, inflammatory mediators such as nitric oxide (NO) and prostaglandin E2, and pro-inflammatory cytokines, including tumor necrosis factor α and interleukin-6, in a dose-dependent manner without cytotoxicity (P < 0.001). Black soybean anthocyanins downregulated the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated RAW 264.7 cells (P < 0.001). Moreover, black soybean anthocyanins inhibited LPS-induced phosphorylation of MAPKs, including extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 (P < 0.001).
CONCLUSION: These results suggest that black soybean anthocyanins exert anti-inflammatory activity by inhibiting ROS generation and subsequent MAPKs signaling, thereby inhibiting inflammatory responses.

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INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2018-594-001320494